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Butyrate induces selective transcriptional activation of a hypomethylated
embryonic globin gene in adult erythroid cells
LJ Burns, JG Glauber and GD Ginder
Department of Internal Medicine, University of Iowa College of Medicine,
Iowa City 52242.
An animal model of hemoglobin switching has been developed in which anemic
adult chickens are treated with 5-azacytidine and sodium butyrate or
alpha-aminobutyric acid, thereby resulting in activation of the embryonic
rho-globin gene in adult erythroid cells. In vitro nuclear runoff
transcription assays using erythroid nuclei from treated birds show that
the mechanism of activation of the rho-globin gene is transcriptional
whereas no transcriptional activation of the embryonic epsilon-globin gene
occurs. The action of 5-azacytidine appears to be as an inhibitor of DNA
methylation because other S-phase active cytotoxic drugs, when substituted
for 5-azacytidine, do not cause demethylation of the embryonic globin
genes, nor do they allow transcriptional activation to occur. Embryonic
rho-globin gene activation in this model is not due to selection of
primitive erythroid cells since a subpopulation of primitive erythroid
cells is not evident either morphologically or when cells are probed for
embryonic and adult globin RNA by in situ hybridization. These studies show
that demethylation by 5-azacytidine is a prerequisite but not sufficient
cis- regulatory event for a high level of transcriptional activation of the
embryonic rho-globin gene in adult erythroid cells in vivo. The possible
basis for the selective transcriptional activation by sodium butyrate in
this system is discussed.
Volume 72,
Issue 5,
pp. 1536-1542,
11/01/1988
Copyright © 1988 by The American Society of Hematology
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